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TIME-AND DOSE-DEPENDENT UP-REGULATION OF TNF-α mRNA AFTER IRRADIATION OF HUMAN NSCLC CELL LINES IN VITRO
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作者 刘莉 CE Ruebe Ch Ruebe 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2006年第1期19-25,共7页
Objective: Even though radiotherapy plays a major role in the local treatment of non-small cell lung cancer (NSCLC), little is known about the molecular effects of irradiation in this tumor. In the present study, w... Objective: Even though radiotherapy plays a major role in the local treatment of non-small cell lung cancer (NSCLC), little is known about the molecular effects of irradiation in this tumor. In the present study, we examined two NSCLC cell lines for their endogenous production of TNF-α after irradiation. To investigate the radiation-induced TNF-α production in NSCLC cell lines. Methods: Two human NSCLC cell lines (A549: squamous; NCI-H596: adenosquamous) were investigated for their TNF-α mRNA (real-time RT-PCR) after exposure to different irradiation doses (2, 5, 10, 20, 30, 40 Gy) and time intervals (1, 3, 6, 12, 24, 48 or 72 h). The TNF-α mRNA expression was quantified by real-time RT-PCR. The clonogenic survival was evaluated after irradiation with 2, 4, 6 and 8 Gy. Results: Non-irradiated NSCLC cells exhibited no or very low TNF-α expression. For the NCI-H596 cell line, TNF-α expression was significantly elevated 1~12 h (maximum 6h: 568fold increase relative to unirradiated cells) in a time-dependent manner. The radiation-induced increase could be observed after irradiation with 2 Gy reaching maximal at 40 Gy, with 83 times higher than normal controls. The clonogenic survival of these cell lines was nearly identical. Conclusion: NCI-H596 cells produce significant quantities of TNF-α following irradiation in a time- and dose-dependent manner. The pro-inflammatory cytokine TNF-α is a key mediator for the pathogenesis of radiation pneumonitis. Radiation-induced endogenous TNF-α expression in NSCLC cells may affect the normal lung adjacent to the tumor and may be associated with an adverse clinical outcome of the patient. 展开更多
关键词 Bronchial tumor cell lines a549 NCI-h596) Tumor necrosis factor (TNF-α) Ionizing radiation
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Study of ATP borate ester effects on cell sensitization to radiation emitted by a nuclear reactor 被引量:1
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作者 Miao Wang Yong-Peng Tong +1 位作者 Qi Luo Shi-Peng Hu 《Nuclear Science and Techniques》 SCIE CAS CSCD 2020年第1期13-25,共13页
Adenosine triphosphate(ATP)borate ester as a new boron agent for boron neutron capture therapy was tested.It was synthesized via a dehydration reaction induced by heating adenosine triphosphate disodium with boric aci... Adenosine triphosphate(ATP)borate ester as a new boron agent for boron neutron capture therapy was tested.It was synthesized via a dehydration reaction induced by heating adenosine triphosphate disodium with boric acid.Next,ATP borate ester pretreatments were assessed to study their effects on cell sensitization from exposure to thermal neutron irradiation emitted by a nuclear reactor.Using cell viability assays(CCK8),survival rates of A549 cells pretreated with or without boroncontaining agents,including ATP borate ester and 4-dihydroxyborylphenylalanine(BPA),were measured.One week after feeding an ATP borate ester solution to tumorbearing nude mice,elemental B content values of tumor muscle and blood were measured using inductively coupled plasma mass spectrometry(ICP-MS).Meanwhile,other tumor tissue samples were placed in a culture medium,subjected to a 3-min neutron irradiation exposure,and then fixed in formalin 24 h later for the terminaldeoxynucleotidyl transferase(TDT)-mediated d UTP nick end labeling(TUNEL)immunohistochemical staining analysis.Results showed that A549 cell irradiation sensitization(irradiation dose of 0.33 Gy)varied with pretreatment.Sensitization values of the ATP borate ester pretreatment group were 1.3–14.1 with boron agent concentrations of 0.3–4.5 mM.Within 1.1–3.4 mM,ATP borate ester showed significantly higher sensitization values than BPA.Meanwhile,TUNEL results demonstrated that apoptosis rates of tumor tissue cells exposed to irradiation after ATP borate ester pretreatment significantly exceeded the corresponding rates for BPA-pretreated cells.In animal experiments,although the distribution ratio of ATP borate ester(tumor tissue/normal muscle,T/N)of 1.2 was not significantly different compared with that of BPA(1.3),the total ATP borate ester concentration in the tumor tissue(0.79±0.05μg/g)significantly exceeded that of BPA(0.58±0.05μg/g).Thus,compared with BPA,the greater enrichment of ATP borate ester in tumor tissues permits preferential targeting toward tumor cells for radiation sensitization.Therefore,ATP borate ester is superior to BPA for use in boron neutron capture therapy. 展开更多
关键词 ATP borate ester Boron agent Neutron radiation Sensitizing effect a549 cell lines
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TGF-β/Akt/Smad signaling regulates ionizing radiation-induced epithelial-mesenchymal transition in acquired radioresistant lung cancer cells 被引量:1
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作者 Yongchun Zhou Lingli Liao +6 位作者 Nan Su Hua Huang Yaoguo Yang Yan Yang Gengming Wang Hongbo Xu Hao Jiang 《Radiation Medicine and Protection》 2022年第3期139-145,共7页
Objective:To define the properties of lung cancer cells that resisted conventionally fractionated radiation exposure.Methods:Acquired radioresistant lung cancer cell line A549 was constructed by X-ray irradiation with... Objective:To define the properties of lung cancer cells that resisted conventionally fractionated radiation exposure.Methods:Acquired radioresistant lung cancer cell line A549 was constructed by X-ray irradiation with a clinical conventional fraction dose of 2 Gy daily during 30 fractions.Cell morphology,molecular markers,migration capacity and invasion potential were evaluated by the microscope,Western blot,immunofluorescence,wound healing test and transwell chamber assay,respectively.Results:Radioresistant A549 cells shifted from an epithelial to a mesenchymal morphology,termed as epithelial-mesenchymal transition(EMT),and was accompanied by decreased expressions of epithelial markers(F=4.568,P<0.05)and increased expression of mesenchymal markers(F=4.270,P<0.05),greater migratory and invasive capabilities(t=6.386,5.644,P<0.05).The expression of TGF-β,and phosphorylated levels of Akt and Smad3 were also enhanced(F=6.496,4.685,3.370,P<0.05).Furthermore,the EMT phenotype induced by radiation could be reversed through inhibition of TGF-β,Akt or Smad3,indicating a functional relationship be-tween them.Conclusions:EMT mediates acquired radioresistance of lung cancer cells induced by IR with clinical parameters,and the crosstalk mode of TGF-β/Akt/Smad signaling plays a critical regulatory role in this process. 展开更多
关键词 Ionizing radiation Acquired radioresistance Epithelial-mesenchymal transition Lung cancer cell line a549 Transforming growth factor-beta/Smad/Akt
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